ライフサイエンスコーパス: periodontal

1 The delayed root formation and periodontal abnormalities may be related to defects in R

2 In 2017 the World Workshop on Periodontal and Peri-implant Diseases and Conditions est

3 natives to autogenous soft tissue grafts for periodontal and peri-implant plastic surgical reconstruc

4 ations of ECM-based scaffold technologies in periodontal and peri-implant soft tissue augmentation wh

5 Periodontal and peri-implant status were assessed based

6 l review of the current knowledge concerning periodontal and periapical lesions activity and the unde

7 Periodontal and periapical lesions are infectious inflam

8 rom clinical and preclinical studies of both periodontal and periapical lesions points to a high rece

9 A clinical periodontal assessment was performed, including bleeding

10 se cells leads to defective formation of the periodontal attachment apparatus, tooth root malformatio

11 of the highly functional tooth root and the periodontal attachment apparatus, while facilitating for

12 nced new bone formation and more significant periodontal attachment were observed in the DPSC + THSG

13 In one model, periodontal bacteria gain access to the systemic circula

14 ned dysbiotic proinflammatory environment by periodontal bacteria may serve to functionally link peri

15 These results suggest that periodontal bacterial infection may cause significant ch

16 rism patterning, and spontaneous age-induced periodontal bone and root loss are observed in this mous

17 eriodontal bone, attenuation of gingival and periodontal bone inflammation, and revertive shift of th

18 egulated matrix metalloproteinase-8, whereas periodontal bone level and the expressions of vascular e

19 in significantly restricted ligature-induced periodontal bone loss (P <0 .01) and suppressed the leve

20 Periodontal bone loss was measured via histological and

21 ge-associated disorder clinically defined by periodontal bone loss, inflammation of the specialized t

22 sion) in which there is a furcal lesion with periodontal bone loss; Group I (intermediate) in which t

23 The periodontal bone supporting ratio in site with DPSC + TH

24 y of elderly mice, including regeneration of periodontal bone, attenuation of gingival and periodonta

25 The clinical and periodontal characteristics, serum, and saliva samples w

26 After a full periodontal clinical assessment, GCF samples were collec

27 Periodontal clinical parameters and esthetics were evalu

28 Periodontal clinical parameters were recorded as well as

29 All periodontal clinical parameters were significantly highe

30 the number of cigarettes consumed (NCC), on periodontal clinical parameters.

31 The periodontal complex includes 2 mineralized tissues, ceme

32 s an association between the severity of the periodontal condition and AMI, suggesting a possible rel

33 The study participants' periodontal condition was examined both in the Health 20

34 duals presented lower rates of RP and better periodontal condition when compared to BDF individuals.

35 to test the independent association between periodontal conditions and serum hsCRP levels.

36 Baseline periodontal data from a full-mouth periodontal exam (N =

37 nistered omega-3 PUFA and ASA as adjuncts to periodontal debridement for the treatment of periodontit

38 Adjunctive omega-3 and ASA after periodontal debridement provides clinical and immunologi

39 cells (DPSC) on the healing of experimental periodontal defects in rats.

40 were extracted, and after healing, bilateral periodontal defects were surgically created mesially in

41 esses were observed when assessing intrabony periodontal defects.

42 At the onset of periodontal development, progenitor cell populations suc

43 fluid (GCF) during early pregnancy with the periodontal diagnosis and the risk of GDM development.

44 is is supported by the fact that severity of periodontal disease (CAL) is associated with the presenc

45 sleeping are 40% less likely to have severe periodontal disease (odds ratio [OR] = 0.6, P < 0.05), a

46 of the relationship between sleep and severe periodontal disease (OR = 4.8, P < 0.05).

47 Periodontal disease (PD) has been suggested to be a risk

48 Periodontal disease (PD) is known to be associated with

49 ctive associations among Hp sero-positivity, periodontal disease (Pd), and infections with incident A

50 tween home use of flossing and prevalence of periodontal disease and caries in older adults.

51 studies have shown the relationship between periodontal disease and chronic kidney disease, but ther

52 cal conditions may worsen the course of both periodontal disease and CKD.

53 ndings show the importance of evaluating the periodontal disease and detecting herpesviruses in patie

54 that oral diseases such as dental caries and periodontal disease and general health conditions such a

55 ntal bacteria may serve to functionally link periodontal disease and oral cancer.

56 studies of pregnant women have demonstrated periodontal disease as a risk factor for preterm birth,

57 ollow-Up Study, who were healthy and free of periodontal disease at baseline (1986).

58 cally significantly associated with clinical periodontal disease at baseline, were examined with dise

59 on of periodontal diseases aimed to identify periodontal disease based on a multidimensional staging

60 ficantly associated with a specific stage of periodontal disease characterized by severe tooth loss,

61 ecting subgingival calculus in patients with periodontal disease compared with photographic assessmen

62 ignificantly associated with the presence of periodontal disease during pregnancy.

63 Periodontal disease has been linked to coronary heart di

64 ntion targets to prevent systemic effects of periodontal disease if further studies establish a causa

65 e the association between sleep duration and periodontal disease in a national US population study in

66 steoporosis or osteopenia is associated with periodontal disease in a population of adult women.

67 g that it may be a useful tool for screening periodontal disease in different populations; yet they h

68 inal study was to evaluate the recurrence of periodontal disease in obese and normal weight patients

69 tentially rejuvenate oral health and reverse periodontal disease in the elderly.

70 her chronic comorbidities, the prevalence of periodontal disease increases with aging.

71 atment strategies for CVD and may inform how periodontal disease influences CVD.

72 Periodontal disease involves an inflammatory destructive

73 This concept suggests that periodontal disease is a group of distinct conditions.

74 Periodontal disease is an age-associated disorder clinic

75 Biologically informed stratification of periodontal disease is both feasible and desirable.

76 A second shift in periodontal disease is taking place.

77 Active periodontal disease may result in downregulation of infl

78 ion, using an in vivo P. gingivalis-mediated periodontal disease model, we show that JAK3 inhibition

79 l shift in our understanding of the basis of periodontal disease occurred early in the 2000s.

80 how variants of IFI16 and AIM2 contribute to periodontal disease pathogenesis may lead to treatment o

81 ey proinflammatory cytokines associated with periodontal disease pathogenesis.

82 sociation between subgingival microbiota and periodontal disease progression in older women, for whic

83 Inflammatory conditions as they occur during periodontal disease result in unique histone methylation

84 Microbial dysbiosis that occurs in periodontal disease results from a hyperinflammatory sta

85 with oxidative stress; however, its role in periodontal disease still remains elusive.

86 tions seeking to unveil the genomic basis of periodontal disease susceptibility.

87 ngoing clinical trial testing the benefit of periodontal disease treatment as a strategy to reduce ri

88 Recent epidemiological studies link Periodontal disease(PD) to age-related macular degenerat

89 association has been reported between RA and periodontal disease, and Porphyromonas gingivalis, a kno

90 Currently, there is no therapy for reversing periodontal disease, and treatment is generally restrict

91 n addition to a positive association between periodontal disease, dental caries, and cocaine use, sel

92 In periodontal disease, inflammation, and microbial dysbios

93 administration preserves bone volume during periodontal disease, repairs bone defects surrounding de

94 ors represents a potential strategy to treat periodontal disease.

95 -1 has a pro-resorptive role in experimental periodontal disease.

96 t were associated with increased severity of periodontal disease.

97 al and systemic inflammation associated with periodontal disease.

98 verages could potentially impact the risk of periodontal disease.

99 m, is now a proposed diagnostic indicator of periodontal disease.

100 ied the association between sleep and severe periodontal disease.

101 crease the activity of NLRP3 and IL-1beta in periodontal disease.

102 The most investigated outcomes were periodontal diseases (42%) and oral cancers (30%).

103 A new classification of periodontal diseases aimed to identify periodontal disea

104 Periodontal diseases can lead to chronic inflammation af

105 erate/severe) (n = 55) according to the 2017 Periodontal Diseases Classification.

106 The new classification of periodontal diseases recognizes the key role of the inte

107 This is particularly true of periodontal diseases that relate to many systemic diseas

108 and disease, with specific focus on caries, periodontal diseases, and cancer.

109 These parameters are related to periodontal diseases, which are directly and indirectly

110 partite motif-containing (TRIM) proteins, in periodontal diseases.

111 (APE) are assumed to be more susceptible to periodontal diseases.

112 mically healthy individuals with and without periodontal diseases.

113 ts microbiota and increase susceptibility to periodontal diseases.

114 P; group-3: Non-diabetic individuals without periodontal diseases.

115 teocytes contributes to deterioration of the periodontal environment by exacerbating chronic inflamma

116 Baseline periodontal data from a full-mouth periodontal exam (N = 6,300) and CHD outcomes through 20

117 A complete maternal/obstetric and periodontal exam was performed, and GCF samples were obt

118 t changed to a worse prognosis at the latest periodontal exam.

119 a brief patient interview and an abbreviated periodontal examination accurately identifies individual

120 Full-mouth periodontal examination and oral hygiene habits were eva

121 Dentate individuals underwent a full-mouth periodontal examination at six sites/tooth.

122 Two 24-h dietary recalls and periodontal examination data from the cross-sectional US

123 participants were submitted to a full-mouth periodontal examination to determine the occurrence of p

124 ndividuals, aged >=30 years, who completed a periodontal examination, in the 2009 to 2014 National He

125 ine and hip bone densitometry and a complete periodontal examination.

126 Data were derived from periodontal examinations performed on 66 adult subjects.

127 ulate the expression of MMPs associated with periodontal extracellular matrix degradation.

128 week-interval, performed with ultrasonic and periodontal hand instruments.

129 es) were divided into four groups, including periodontal health (H), gingivitis (G), chronic periodon

130 procalcitonin (PCT) to differentiate between periodontal health and Stage II and III periodontitis.

131 may have important esthetic, functional, and periodontal health implications.

132 otics may improve the known deterioration of periodontal health in navy sailors during deployments at

133 efficacious measure to improve and maintain periodontal health in situations with waning efficacy of

134 ng thin phenotype into a thick phenotype for periodontal health maintenance.

135 sites without mucogingival defects help with periodontal health maintenance?

136 cting "proinflammatory" salivary profile and periodontal health status in adolescents.

137 molecular therapeutic for the restoration of periodontal health through the inhibition of NF-kappaB a

138 ficacy in augmenting KT, GT and in improving periodontal health using autogenous, allogenic, and xeno

139 ignificantly greater improvements in overall periodontal health with less frequent BoP and a higher n

140 ease might benefit from UDCA with respect to periodontal health.

141 ing functions, which are critical to support periodontal health.

142 r UDCA holds anti-inflammatory properties on periodontal health.

143 re divided into groups: (H) systemically and periodontal healthy (control group); (P) with periodonti

144 he Periodontal Inflamed Surface Area and the Periodontal Index for Risk of Infectiousness (PIRI).

145 ontal prediction model (PPM) including three periodontal indicators (missing teeth, percentage of sit

146 critically needed to counter the sources of periodontal infection and inflammation that are accelera

147 ical parameters were recorded as well as the Periodontal Inflamed Surface Area and the Periodontal In

148 ay an important role both in the presence of periodontal inflammation during pregnancy and subsequent

149 Here, we report that periodontal inflammation exacerbates gut inflammation in

150 expected therapeutic targets for alleviating periodontal inflammation in people with T2D.

151 These findings support the idea that periodontal inflammation promotes metastasis of breast c

152 naling molecules that trigger and perpetuate periodontal inflammation.

153 ked by periodontitis-related bacteria and/or periodontal inflammation.

154 involvement in myeloid cell functions during periodontal inflammation.

155 reuteri) treatment towards the reduction in periodontal inflammatory parameters (clinical attachment

156 y and the survival of the treated teeth with periodontal infrabony defects.

157 Periodontal intervention studies are warranted.

158 ness, may affect linear bone measurements of periodontal intrabony defects.

159 Recent studies revealed culturable periodontal keystone pathogens are associated with prete

160 The viability and behaviors of periodontal ligament (PDL) cells on nanofibers, and anti

161 Breakdown of the JE barrier results in periodontal ligament (PDL) disintegration, alveolar bone

162 developing teeth and in odontoblasts and the periodontal ligament (PDL) of adults.

163 Teeth are attached to alveolar bone by the periodontal ligament (PDL), which contains stem cells su

164 rocess: unmineralized collagen fibers of the periodontal ligament anchor directly into the outer laye

165 Human periodontal ligament cells (hPDL cells) express several

166 Human periodontal ligament cells (hPDLCs) are regulated by vit

167 rentiation of those cells, and comparison of periodontal ligament mesenchymal stem cells (PDLMSCs) an

168 ited information on their effects during the periodontal maintenance phase.

169 the recurrence of periodontitis (RP) during periodontal maintenance therapy (PMT) programs have not

170 t methods to treat persistent pockets during periodontal maintenance therapy (PMT) require further in

171 ry outcomes compared with PR/RP alone during periodontal maintenance therapy.

172 This study showed that periodontal measurements could play a role in identifyin

173 with diabetes, and that addition of clinical periodontal measurements improved the performance of FIN

174 ntal treatment was performed and whole-mouth periodontal measurements were recorded at baseline, 1, 3

175 Clinical periodontal measurements were recorded; periodontitis pa

176 There is a sparsity of data describing the periodontal microbiome in elderly individuals.

177 usters of IgG antibodies against 19 selected periodontal microorganisms have been associated with hyp

178 th clinical examination of the assessment of periodontal, mucosal, and oral health.

179 When compared with dental pulp cells, periodontal neural crest lineage differentiation is char

180 ing postoperative medications to the type of periodontal/oral surgery performed will help prevent ove

181 l of perceived pain after different types of periodontal/oral surgical procedures, and the difference

182 Periodontal outcome measures in 2011 were the number of

183 In all the study participants, clinical periodontal parameters (plaque index, gingival index, su

184 There was no significant difference in periodontal parameters and serum IgG levels for periodon

185 There was no significant difference in periodontal parameters at 3- and 6-month follow-ups in p

186 All periodontal parameters improved in both groups after per

187 GCF samples were collected and clinical periodontal parameters including probing depth, clinical

188 This case-control study assessed complete periodontal parameters of 714 subjects with periodontal

189 toothpaste containing 0.3% triclosan on the periodontal parameters of subjects that have been treate

190 t patients did not differ in relation to the periodontal parameters of VPI, GBI, PD, CAL, or BOP 2 ye

191 Periodontal parameters were comparable but the proportio

192 bgingival plaque were collected and clinical periodontal parameters were recorded.

193 The following periodontal parameters were recorded: visible plaque ind

194 Periodontal parameters, including pocket probing depth,

195 ated Streptococcus mutans as well as several periodontal pathobionts.

196 Porphyromonas gingivalis is a periodontal pathogen implicated in a range of pregnancy

197 lipid 430 and lipid 654, are produced by the periodontal pathogen Porphyromonas gingivalis and can be

198 Here, we demonstrate that infection with the periodontal pathogen Porphyromonas gingivalis enhances t

199 anaerobe, Porphyromonas gingivalis, is a key periodontal pathogen, and several lines of evidence link

200 ously reported that oral administration of a periodontal pathogen, Porphyromonas gingivalis (Pg) to W

201 iodontal parameters and serum IgG levels for periodontal pathogens between PLBW and healthy delivery

202 Increased levels of periodontal pathogens disrupt the homeostasis between th

203 However the mechanisms by which periodontal pathogens influence the development of predi

204 The inflammatory response to periodontal pathogens is dynamically controlled by the c

205 tween Helicobacter pylori (Hp) and groups of periodontal pathogens may alter the onset of Alzheimer's

206 g effects of co-eradication of Hp and select periodontal pathogens on neurodegenerative disease.

207 This study evaluated the levels of periodontal pathogens Prevotella intermedia, Porphyromon

208 newly developed CST can detect five typical periodontal pathogens with a somewhat lower sensitivity

209 Exposures consisted of 19 periodontal pathogens, constructed factors and clusters,

210 Moreover, traditional periodontal pathogens, such as Porphyromonas gingivalis,

211 The periodontal phenotype consists of the bone morphotype, t

212 It was found that periodontal phenotype varies among different individuals

213 provide clinical benefits such as modifying periodontal phenotype, maintaining or enhancing facial b

214 ontium, especially in dentitions with a thin periodontal phenotype.

215 Differential abundance across the periodontal phenotypes was calculated using the R packag

216 hree important parameters used to categorize periodontal phenotypes.

217 es have received a great deal of interest in periodontal plastic procedures.

218 nvestigates whether alcohol use predicts the periodontal pocket development over an 11-year follow-up

219 an inflammatory disease that can lead to the periodontal pocket formation and tooth loss.

220 sistently associated with the development of periodontal pockets (IRRs varied from 0.6 to 1.0).

221 e the number of teeth with deepened (>=4 mm) periodontal pockets and the presence of deepened periodo

222 the differences between shallow and residual periodontal pockets in patients with periodontitis (Stag

223 levels had a significantly higher number of periodontal pockets with >=4 mm (P < 0.001).

224 In summary, in the environment of periodontal pockets, which are bathed in gingival crevic

225 of alcohol use and the number of teeth with periodontal pockets.

226 odontal pockets and the presence of deepened periodontal pockets.

227 -based guidelines would be of benefit to the periodontal practicing community.

228 A periodontal prediction model (PPM) including three perio

229 PP was assessed using transparency of periodontal probe through the gingival margin at midfaci

230 survey questioned prescribing practices for periodontal procedures, prescribing rationale, demograph

231 Periodontitis was defined by the Periodontal Profile Class System adapted to Stages (PPC

232 he treatment of multiple Class III-IV Miller periodontal recession (REC) defects on mandibular anteri

233 iologic-based techniques are able to promote periodontal regeneration coupled with the provision of t

234 of the combination with CM, may improve the periodontal regeneration of dehiscence-type defects in t

235 gesting PP(i) metabolism may be a target for periodontal regenerative therapies.

236 e 4 or Grade C showed a significantly higher periodontal-related tooth loss.

237 ofibers reduced inflammation and accelerated periodontal repair at an early stage, providing good pro

238 elop an antibiotic-loaded membrane to assist periodontal repair.

239 ence (FTND) has received little attention in periodontal research.

240 ent NCC as an indicator of smoking status in periodontal research.

241 le) was assessed by calculating the modified periodontal screening score (mPESS) from selected questi

242 selectively removed from demineralized mouse periodontal sections via enzymatic digestion.

243 and dramatically visualizes the substantial periodontal site-specific differences.

244 rrent smokers had more affected teeth and/or periodontal sites with a different contour pattern than

245 rdental clinical attachment for defining the periodontal status and the extent of disease severity.

246 periodontal parameters of 714 subjects with periodontal status classified as healthy/mild periodonti

247 (2) Stage can shift upward over time, if the periodontal status deteriorates, but the initially assig

248 subgingival bacterial profiles and clinical periodontal status in a cohort of participants in the Wa

249 ofilm control during PMT leading to a better periodontal status maintenance.

250 Periodontal status was classified according to the Cente

251 Poor maternal periodontal status, increased oral inflammatory load and

252 ely examine the association between maternal periodontal status, oral inflammatory load and serum C-

253 ivitis group (PG, n = 70) according to their periodontal status.

254 sive bone and attachment loss and regenerate periodontal structures.

255 stration defects, which can manifest loss of periodontal support and gingival recession (GR).

256 uate practices in antibiotics prescribed for periodontal surgeries with and without bone grafting and

257 ely to prescribe antibiotics for traditional periodontal surgeries without bone grafting compared wit

258 e results, the low incidence of infection in periodontal surgery cited in the literature, and willing

259 During the periodontal surgery gingival biopsies were collected and

260 tal parameters improved in both groups after periodontal surgery.

261 compared with photographic assessment during periodontal surgery.

262 nalyses of publicly available Obstetrics and Periodontal Therapy (OPT) trial data.

263 rivative (EMD) as an adjunct to non-surgical periodontal therapy (test) versus non-surgical therapy a

264 Periodontal therapy during the second trimester improves

265 indings from interventional studies in which periodontal therapy failed to alleviate systemic health

266 Thus, while periodontal therapy may improve oral health, it may be e

267 aluated at two time points: T1 (after active periodontal therapy) and T2 (6 years).

268 CAL, or BOP 2 years after completion of the periodontal therapy.

269 ated the root resorption volume and examined periodontal tissue cathepsin K, Runx2, TNF-alpha, and IL

270 in significantly limits the ligature-induced periodontal tissue destruction (P <0.01).

271 vitamin D(3) and play a fundamental role in periodontal tissue homeostasis and inflammatory response

272 assess the impact of the amount of inflamed periodontal tissue on the levels of systemic inflammator

273 Periodontal tissue response was assessed by histomorphom

274 an be detected in lipid extracts of diseased periodontal tissues and teeth of humans.

275 extracellular matrix molecules expressed in periodontal tissues are indeed substrates of FAM20C.

276 AM20C is required for maintenance of healthy periodontal tissues.

277 exacerbation of the inflammatory response in periodontal tissues.

278 study included 22 patients who had received periodontal treatment 2 years previously, 13 obese and n

279 m LRG, IL-6 and TNF-alpha was detected after periodontal treatment compared with baseline values of p

280 IV, Grade C respond well to the non-surgical periodontal treatment during the 6-month follow-up.

281 OLS models to evaluate SACE for periodontal treatment effects on birthweight and gestati

282 or for periodontitis, supplementation during periodontal treatment has not been shown to be beneficia

283 th of robust evidence on whether nonsurgical periodontal treatment improves systemic disease outcomes

284 has an effect on the outcome of non-surgical periodontal treatment in patients with chronic periodont

285 Volunteers who received periodontal treatment in the aforementioned RCT were sel

286 s estimating SACE to calculate the effect of periodontal treatment on birthweight and gestational age

287 y aimed to assess the effect of non-surgical periodontal treatment on gingival crevicular fluid (GCF)

288 study analyzed the influence of non-surgical periodontal treatment on serum levels of MBL and SIRT1.

289 views that studied the effect of nonsurgical periodontal treatment on systemic disease outcomes.

290 -analyses (MAs) have evaluated the effect of periodontal treatment on systemic outcomes.

291 Because periodontal treatment reduces inflammation in oral tissu

292 Periodontal treatment was associated with decreased seru

293 Conventional quadrant-wise non-surgical periodontal treatment was performed and whole-mouth peri

294 periodontitis patients received non-surgical periodontal treatment, and GCF and serum samples were ob

295 to 1.66 +/- 1.64 ng/mL; P < 0.001) following periodontal treatment.

296 eness of vitamin D(3) supplementation during periodontal treatment.

297 titis (Stages III and IV) after non-surgical periodontal treatment.

298 periodontitis before and after non-surgical periodontal treatment.

299 The results revealed a higher prevalence of periodontal viruses such as EBV and CMV in CAD patients

300 Periodontal viruses such as EBV and CMV were significant

301 gressively gained popularity in the field of periodontal wound healing and regeneration.